Formation of lipoidal derivatives of estradiol-17 beta (E2) esterified to long-chained fatty acids has been reported to occur in estrogen target tissues. Employing human breast cancer cells in culture, we have detected the rapid synthesis of such compounds upon exposure of the cells to concentrations of [3H]E2 as low as 1 nM. When exposed to 10 nM [3H]E2 in the culture medium, synthesis of E2-lipoidal derivative (E2-L) reached 270 fmol/mg DNA in 2 h in the estrogen receptor positive MCF-7 human mammary cancer cell line. Higher rates (approximately 900 fmol/mg DNA in 2 h) were reached in 2 estrogen receptor negative human mammary cancer cell lines; MDA-MB-231 and MDA-MB-330. E2-L was the major form of estrogen in the latter cells at this time interval (E2-L/E2 approximately 3.0). Far higher concentrations of E2 were found in MCF-7 cells compared to 231 and 330 cells, and, in contrast to the latter, this was mostly specifically bound. Upon subsequent withdrawal of E2 from the medium, intracellular concentrations of E2-L decreased very rapidly in the first 5 h period, then declined more slowly to approximately 50 fmol/mg DNA at 24 h. Intracellular concentrations of E2 were maintained over this time period. E2-L was not present in the medium. Thus, accumulation of E2-L in cells upon continuous exposure to E2 represents the net result of esterification and deesterification reactions. These hydrophobic E2-derivatives may then be involved in the "capture" of E2 for transport through membranes and subsequent regeneration of E2 to maintain occupancy of the nuclear receptor.

Ecchymosis of the scrotum and lower abdominal wall occurred in four newborn boys. All were anemic. Three had coagulation abnormalities and evidence of sepsis. In two, group B streptococcal septicemia was documented. Intraperitoneal hemorrhage from a ruptured subcapsular hematoma of the liver was the source of blood in the scrotum in three, and most probably in the fourth as well. Two infants died in spite of antibiotics, vigorous blood replacement, including exchange transfusion, and desperation laparotomies for continued intraperitoneal hemorrhage. Newborns with scrotal ecchymosis should be examined for intraperitoneal hemorrhage, ruptured subcapsular hematoma of the liver being the most probable source. Their coagulation status should also be evaluated, and sepsis should be suspected, especially in those with a demonstrated coagulopathy. Group B Streptococcus is a likely primary etiologic agent in these critically ill neonates. Nonoperative treatment, as given the two survivors in this experience, is preferred.

The postneonatal infant mortality (PNIM) of 2,205 infants admitted to a neonatal intensive care unit from January 1971 to December 1974 was 44 in 1,000 infants who survived to age 28 days. This rate is approximately ten times that of the general population. Congenital malformations (59%), infections (12%), sudden infant death syndrome (10%), and asphyxial brain damage (10%) were the most common causes of death. One third (26) of the infants remained in the hospital whereas two thirds (52) had been dismissed prior to death. All who remained in the hospital plus 36 who had been dismissed died of severe illnesses that were incompatible with prolonged survival. The remaining PNIM was 10 in 1,000 neonatal survivors. This rate is still twice that of the general population. These deaths occurred in infants who were apparently well at the time of dismissal and subsequent examinations. Sudden infant death syndrome and infections constituted the largest portion of this mortality. Factors contributing to mortality in this group were poor socioeconomic status and low birth weight. Maternal age, race, marital status, and neonatal illnesses including apnea were not significantly related. Factors that appear to be important in the birth of high-risk infants continued to be operative in the postneonatal period, and contribute to a high mortality in apparently normal infants dismissed from the neonatal intensive care unit.

PULMONARY INTERSTITIAL EMPHYSEMA is a frequent complication of idiopathic respiratory distress syndrome in the premature infant?, 2 In many cases the interstitial pulmonary air dissects alongperibronchi al and perivascular spaces leading to pneumomediastinu m or pneumothorax, and less commonly to pneumopericardium or pneumoperitoneum . In rare cases, interstitial pulmonary air may lead to massive inflation of one lung or lobe with tension causing shift of the mediastinum to the opposite side and compression of the contralateral lung?, 4 In such instances the prevailing dynamics are similar to those of congenital lobar emphysema. Two recent publications recommend lobectomy for the treatment of localized PIE under tension?, 4